TNF-α-treated adipocytes shows a significant 64% decrease in insulin-stimulated glucose uptake, whereas Infliximab (10 ng/mL) reverses TNF-α actions by significantly improving glucose incorporation in 3T3L1 adipocytes. Infliximab restores phosphorylation of substrate-2 and AKT by attenuating protein-tyrosine phosphatase 1B (PTP1B) activation. Infliximab ameliorates TNF-α-induced insulin resistance in 3T3L1 adipocytes in vitro by restoring the insulin signalling pathway via PTP1B inhibition.

A single injection of Infliximab (10 μg/g in 100 μl saline/dose ip) in diabetic TNF-α ^+/+ ) mice leads to suppression of the increased serum TNF-α and amelioration of the electrophysiological and biochemical deficits for at least 4 weeks. The increased TNF-α mRNA expression in diabetic dorsal root ganglion is also attenuated by Infliximab.